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Epigenetics and Molecular Genetics of Cancer
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Epigenetics and Molecular Genetics of Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 6322

Special Issue Editor

Dr. Carmen Cristina Diaconu

E-Mail Website
Guest Editor
Stefan S. Nicolau Institute of Virology, Romanian Academy, 030304 Bucharest, Romania
Interests: proteome; secretome; biomarkers; molecular mechanisms of diseases; GPCRs

Special Issue Information

Dear Colleagues, 

Cancer results from the disruption of the balance of cell growth and cell death that is driven by genetic and epigenetic alterations. The molecular profiling of cancer, especially after the emergence of Next-Generation Sequencing technologies, was a huge leap in understanding carcinogenesis, the development of biomarkers for early diagnosis and the development of targeted treatments.

Since most cancers are sporadic, we are still far from understanding the whole complexity of the molecular mechanisms, genes and epigenetic regulators that play a role in cancer development and that have the potential to be exploited as biomarkers for diagnosis, prognosis, personalized therapy targets and the prediction of treatment response.

Another important challenge is to comprehend the role of environmental factors in the modulation of the epigenome and how we can use this knowledge in cancer prevention.

In this context, the aim of this Special Issue of IJMS is to assemble the most relevant works on the epigenetics and molecular genetics mechanisms involved in cancer development, and on how these mechanisms are modulated and can be exploited for the development of more effective treatment strategies.

Dr. Carmen Cristina Diaconu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • molecular genetics mechanisms
  • epigenetic modulation
  • environmental modulation of the epigenome
  • epigenetic regulators
  • cancer prevention

Published Papers (3 papers)

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Research

16 pages, 2396 KiB  
Article
PGC7 Regulates Genome-Wide DNA Methylation by Regulating ERK-Mediated Subcellular Localization of DNMT1
by Xing Wei, Yingxiang Liu, Weijie Hao, Peiwen Feng, Lei Zhang, Hongni Xue, Qunli Zhou and Zekun Guo
Int. J. Mol. Sci. 2023, 24(4), 3093; https://doi.org/10.3390/ijms24043093 - 4 Feb 2023
Cited by 1 | Viewed by 1775
Abstract
DNA methylation is an epigenetic modification that plays a vital role in a variety of biological processes, including the regulation of gene expression, cell differentiation, early embryonic development, genomic imprinting, and X chromosome inactivation. PGC7 is a maternal factor that maintains DNA methylation [...] Read more.
DNA methylation is an epigenetic modification that plays a vital role in a variety of biological processes, including the regulation of gene expression, cell differentiation, early embryonic development, genomic imprinting, and X chromosome inactivation. PGC7 is a maternal factor that maintains DNA methylation during early embryonic development. One mechanism of action has been identified by analyzing the interactions between PGC7 and UHRF1, H3K9 me2, or TET2/TET3, which reveals how PGC7 regulates DNA methylation in oocytes or fertilized embryos. However, the mechanism by which PGC7 regulates the post-translational modification of methylation-related enzymes remains to be elucidated. This study focused on F9 cells (embryonic cancer cells), which display high levels of PGC7 expression. We found that both knockdown of Pgc7 and inhibition of ERK activity resulted in increased genome-wide DNA methylation levels. Mechanistic experiments confirmed that inhibition of ERK activity led to the accumulation of DNMT1 in the nucleus, ERK phosphorylated DNMT1 at ser717, and DNMT1 Ser717-Ala mutation promoted the nuclear localization of DNMT1. Moreover, knockdown of Pgc7 also caused downregulation of ERK phosphorylation and promoted the accumulation of DNMT1 in the nucleus. In conclusion, we reveal a new mechanism by which PGC7 regulates genome-wide DNA methylation via phosphorylation of DNMT1 at ser717 by ERK. These findings may provide new insights into treatments for DNA methylation-related diseases. Full article
(This article belongs to the Special Issue Epigenetics and Molecular Genetics of Cancer)
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19 pages, 3917 KiB  
Article
HMGA1 Regulates the Expression of Replication-Dependent Histone Genes and Cell-Cycle in Breast Cancer Cells
by Sara Petrosino, Sabrina Pacor, Silvia Pegoraro, Virginia Anna Gazziero, Giulia Canarutto, Silvano Piazza, Guidalberto Manfioletti and Riccardo Sgarra
Int. J. Mol. Sci. 2023, 24(1), 594; https://doi.org/10.3390/ijms24010594 - 29 Dec 2022
Cited by 2 | Viewed by 1839
Abstract
Breast cancer (BC) is the primary cause of cancer mortality in women and the triple-negative breast cancer (TNBC) is the most aggressive subtype characterized by poor differentiation and high proliferative properties. High mobility group A1 (HMGA1) is an oncogenic factor involved in the [...] Read more.
Breast cancer (BC) is the primary cause of cancer mortality in women and the triple-negative breast cancer (TNBC) is the most aggressive subtype characterized by poor differentiation and high proliferative properties. High mobility group A1 (HMGA1) is an oncogenic factor involved in the onset and progression of the neoplastic transformation in BC. Here, we unraveled that the replication-dependent-histone (RD-HIST) gene expression is enriched in BC tissues and correlates with HMGA1 expression. We explored the role of HMGA1 in modulating the RD-HIST genes expression in TNBC cells and show that MDA-MB-231 cells, depleted of HMGA1, express low levels of core histones. We show that HMGA1 participates in the activation of the HIST1H4H promoter and that it interacts with the nuclear protein of the ataxia-telangiectasia mutated locus (NPAT), the coordinator of the transcription of the RD-HIST genes. Moreover, we demonstrate that HMGA1 silencing increases the percentage of cells in G0/G1 phase both in TNBC and epirubicin resistant TNBC cells. Moreover, HMGA1 silencing causes an increase in epirubicin IC50 both in parental and epirubicin resistant cells thus suggesting that targeting HMGA1 could affect the efficacy of epirubicin treatment. Full article
(This article belongs to the Special Issue Epigenetics and Molecular Genetics of Cancer)
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19 pages, 51572 KiB  
Article
TRAF4 Promotes the Proliferation of Glioblastoma by Stabilizing SETDB1 to Activate the AKT Pathway
by Hongyu Gu, Shunqin Zhu, Cheng Peng, Zekun Wei, Yang Shen, Chaoyu Yuan, He Yang, Hongjuan Cui and Liqun Yang
Int. J. Mol. Sci. 2022, 23(17), 10161; https://doi.org/10.3390/ijms231710161 - 5 Sep 2022
Cited by 5 | Viewed by 2102
Abstract
The process of ubiquitination regulates the degradation, transport, interaction, and stabilization of substrate proteins, and is crucial for cell signal transduction and function. TNF receptor-associated factor 4, TRAF4, is a member of the TRAF family and is involved in the process of ubiquitination [...] Read more.
The process of ubiquitination regulates the degradation, transport, interaction, and stabilization of substrate proteins, and is crucial for cell signal transduction and function. TNF receptor-associated factor 4, TRAF4, is a member of the TRAF family and is involved in the process of ubiquitination as an E3 ubiquitin protein ligase. Here, we found that TRAF4 expression correlates with glioma subtype and grade, and that TRAF4 is significantly overexpressed in glioblastoma and predicts poor prognosis. Knockdown of TRAF4 significantly inhibited the growth, proliferation, migration, and invasion of glioblastoma cells. Mechanistically, we found that TRAF4 only interacts with the Tudor domain of the AKT pathway activator SETDB1. TRAF4 mediates the atypical ubiquitination of SETDB1 to maintain its stability and function, thereby promoting the activation of the AKT pathway. Restoring SETDB1 expression in TRAF4 knockdown glioblastoma cells partially restored cell growth and proliferation. Collectively, our findings reveal a novel mechanism by which TRAF4 mediates AKT pathway activation, suggesting that TRAF4 may serve as a biomarker and promising therapeutic target for glioblastoma. Full article
(This article belongs to the Special Issue Epigenetics and Molecular Genetics of Cancer)
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